KRAS and colorectal carcinoma: The distinction of genes along PC2 appeared to be driven by the co-occurrence of their expressed mutations with mutation expression in either KRAS or TP53. Exploratory analysis of genes not designated as oncogenes and/or tumor suppressors, but with frequently expressed mutations, indicated enrichment with gene sets related to mRNA splicing (HNRNPC and PCBP1) and deactivation of β-catenin (TCF7L2 [implicated in CRC as fusion gene target], SOX9, and SOX4; Additional file 2: Figure S3b).